Circulating tumor DNA dynamics reveal KRAS G12C mutation heterogeneity and response to treatment with the KRAS G12C inhibitor divarasib in solid tumors.

Yoonha Choi Neekesh V Dharia Tomi Jun Julie Chang Stephanie Royer-Joo Kenneth K Yau Zoe June Assaf Junko Aimi Smruthy S Sivakumar Meagan Montesion Adrian Sacher Patricia M LoRusso Jayesh Desai Jennifer L Schutzman Zhen Shi

Published in: Clinical cancer research : an official journal of the American Association for Cancer Research (2024)

Across tumor types, the KRAS G12C mutation likely represents a truncal mutation in the majority of patients. Rapid and deep decline in ctDNA tumor fraction was observed in patients responding to divarasib treatment. Early on-treatment dynamics of ctDNA were associated with patient outcomes and tumor response to divarasib treatment.

Keyphrases

circulating tumor
end stage renal disease
chronic kidney disease
newly diagnosed
ejection fraction
gene expression
prognostic factors
combination therapy
circulating tumor cells
single molecule
sensitive detection